• 1.

    Reed SM, Bayly WM & McEachern RB, et al. Equine internal medicine. 2nd ed. Philadelphia: Saunders, 2003;545.

  • 2.

    Pellegrini-Masini A, Bentz AI & Johns IC, et al. Common variable immunodeficiency in three horses with presumptive bacterial meningitis. J Am Vet Med Assoc 2005; 227:114122.

    • Search Google Scholar
    • Export Citation
  • 3.

    Flaminio MJ, LaCombe V. Kohn CW, et al. Common variable immunodeficiency in a horse. J Am Vet Med Assoc 2002; 221:12961302.

  • 4.

    Bernard WV, Cohen D & Bosler E, et al. Serologic survey for Borrelia burgdorferi antibody in horses referred to a mid-Atlantic veterinary teaching hospital. J Am Vet Med Assoc 1990; 196:12551258.

    • Search Google Scholar
    • Export Citation
  • 5.

    Magnarelli LA & Anderson JE Class-specific and polyvalent enzyme-linked immunosorbent assays for detection of antibodies to Borrelia burgdorferi in equids. J Am Vet Med Assoc 1989; 195:13651368.

    • Search Google Scholar
    • Export Citation
  • 6.

    Marcus LC, Patterson MM & Gilfillan RE, et al. Antibodies to Borrelia burgdorferiin New England horses: serologic survey. Am J Vet Res 1985; 46:25702571.

    • Search Google Scholar
    • Export Citation
  • 7.

    CDC. Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR Morb Mortal Wkly Rep 1995; 44:590591.

    • Search Google Scholar
    • Export Citation
  • 8.

    Stricker RB. Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with Lyme disease. Clin Infect Dis 2007; 45:149157.

    • Search Google Scholar
    • Export Citation
  • 9.

    Chang YF, Novosel V & Chang CF, et al. Experimental induction of chronic borreliosis in adult dogs exposed to Borrelia burgdorferi–infected ticks and treated with dexamethasone. Am J Vet Res 2001; 62:11041112.

    • Search Google Scholar
    • Export Citation
  • 10.

    Cadavid D, O'Neill T & Schaefer H, et al. Localization of Borrelia burgdorferi in the nervous system and other organs in a nonhuman primate model of Lyme disease. Lab Invest 2000; 80:10431054.

    • Search Google Scholar
    • Export Citation
  • 11.

    Oksi J, Kalimo H & Marttila RJ, et al. Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. Brain 1996; 119:21432154.

    • Search Google Scholar
    • Export Citation
  • 12.

    Halperin JJ. Neuroborreliosis. Am J Med 1995; 98:52S-56S.

  • 13.

    Kaiser R. Neuroborreliosis. J Neurol 1998; 245:247255.

  • 14.

    Burgess EC, Gillette D, Pickett JP. Arthritis and panuveitis as manifestations of Borrelia burgdorferi infection in a Wisconsin pony. J Am Vet Med Assoc 1986; 189:13401342.

    • Search Google Scholar
    • Export Citation
  • 15.

    Browning A, Carter SD & Barnes A, et al. Lameness associated with Borrelia burgdorferi infection in the horse. Vet Rec 1993; 132:610611.

  • 16.

    Burgess EC, Mattison M. Encephalitis associated with Borrelia burgdorferi infection in a horse. J Am Vet Med Assoc 1987; 191:14571458.

  • 17.

    Bai Y, Narayan K & Dail D, et al. Spinal cord involvement in the nonhuman primate model of Lyme disease. Lab Invest 2004; 84:160172.

  • 18.

    Köchling J, Freitag HJ & Bollinger T, et al. Lyme disease with lymphocytic meningitis, trigeminal palsy and silent thalamic lesion. Eur J Paediatr Neurol 2008; 12:501504.

    • Search Google Scholar
    • Export Citation
  • 19.

    Ramesh G, Borda JT & Dufour J, et al. Interaction of the Lyme disease spirochete Borrelia burgdorferi with brain parenchyma elicits inflammatory mediators from glial cells as well as glial and neuronal apoptosis. Am J Pathol 2008; 173:14151427.

    • Search Google Scholar
    • Export Citation
  • 20.

    Garcia-Monco JC, Fernandez-Villar B, Benach JL. Adherence of the Lyme disease spirochete to glial cells and cells of glial origin. J Infect Dis 1989; 160:497506.

    • Search Google Scholar
    • Export Citation
  • 21.

    Coburn J, Fischer JR, Leong JM. Solving a sticky problem: new genetic approaches to host cell adhesion by the Lyme disease spirochete. Mol Microbiol 2005; 57:11821195.

    • Search Google Scholar
    • Export Citation
  • 22.

    Fikrig E, Narasimhan S. Borrelia burgdorferi—traveling incognito? Microbes Infect 2006; 8:13901399.

  • 23.

    Li L, Narayan K & Pak E, et al. Intrathecal antibody production in a mouse model of Lyme neuroborreliosis. J Neuroimmunol 2006; 173:5668.

  • 24.

    Liang FT, Brown EL & Wang T, et al. Protective niche for Borrelia burgdorferi to evade humoral immunity. Am J Pathol 2004; 165:977985.

  • 25.

    Flaminio MJBF, Tallmadge RL & Salles-Gomes COM, et al. Common variable immunodeficiency in horses is characterized by B cell depletion in primary and secondary lymphoid tissues. J Clin Immunol 2009; 29:107116.

    • Search Google Scholar
    • Export Citation
  • 26.

    Chang YF, Ku YW & Chang CF, et al. Antibiotic treatment of experimentally Borrelia burgdorferi-iniected ponies. Vet Microbiol 2005; 107:285294.

  • 27.

    Bryant JE, Brown MP & Gronwall RR, et al. Study of intragastric administration of doxycycline: pharmacokinetics including body fluid, endometrial and minimum inhibitory concentrations. Equine Vet J 2000; 32:233238.

    • Search Google Scholar
    • Export Citation
  • 28.

    Meli DN, Coimbra RS & Erhart DG, et al. Doxycycline reduces mortality and injury to the brain and cochlea in experimental pneumococcal meningitis. Infect Immun 2006; 74:38903896.

    • Search Google Scholar
    • Export Citation
  • 29.

    Kim D, Kordick D & Divers T, et al. In vitro susceptibilities of Leptospira spp. and Borrelia burgdorferi isolates to amoxicillin, tilmicosin, and enrofloxacin. J Vet Sci 2006; 7:355359.

    • Search Google Scholar
    • Export Citation
  • 30.

    Clark C, Dowling PM & Ross S, et al. Pharmacokinetics of tilmicosin in equine tissues and plasma. J Vet Pharmacol Ther 2007; 31:6670.

  • 31.

    Klempner MS, Hu LT & Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med 2001; 345:8592.

    • Search Google Scholar
    • Export Citation
  • 32.

    Oksi J, Nikoskelainen J & Hiekkanen H, et al. Duration of antibiotic treatment in disseminated Lyme borreliosis: a double-blind, randomized, placebo-controlled, multicenter clinical study. Eur J Clin Microbiol Infect Dis 2007; 26:571581.

    • Search Google Scholar
    • Export Citation
  • 33.

    Wormser GP, Ramanathan R & Nowakowski J, et al. Duration of antibiotic therapy for early Lyme disease. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 2003; 138:697704.

    • Search Google Scholar
    • Export Citation
  • 34.

    Auwaerter PG. Point: antibiotic therapy is not the answer for patients with persisting symptoms attributable to Lyme disease. Clin Infect Dis 2007; 45:143148.

    • Search Google Scholar
    • Export Citation
  • 35.

    Krupp LB, Hyman LG & Crimson R, et al. Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial. Neurology 2003; 60:19231930.

    • Search Google Scholar
    • Export Citation
  • 36.

    Wormser GP, Nadelman RB & Dattwyler RJ, et al. Practice guidelines for the treatment of Lyme disease. The Infectious Diseases Society of America. Clin Infect Dis 2000; 31(suppl 1):114.

    • Search Google Scholar
    • Export Citation

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Meningitis, cranial neuritis, and radiculoneuritis associated with Borrelia burgdorferi infection in a horse

Frances M. James MAVetMB, DACVS1, Julie B. Engiles VMD, DACVP2, and Jill Beech VMD, DACVIM3
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  • 1 Departments of Clinical Studies, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348.
  • | 2 Departments of Pathobiology, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348.
  • | 3 Departments of Clinical Studies, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348.

Abstract

Case Description—A 12-year-old Thoroughbred was examined because of signs of depression, neck stiffness, and poor performance.

Clinical Findings—Physical examination revealed that the horse was dull, appeared depressed, was reluctant to raise its neck and head above a horizontal plane, and had a temperature of 38.5°C (101.3°F). No radiographic or scintigraphic abnormalities of the neck were found; however, high plasma fibrinogen concentration and relative lymphopenia were identified and the horse was seropositive for antibodies against Borrelia burgdorferi. Analysis of CSF revealed neutrophilic inflammation, and results of a PCR assay of CSF for B burgdorferi DNA were positive. Immunologic testing revealed severe B-cell lymphopenia and a low serum IgM concentration consistent with common variable immunodeficiency.

Treatment and Outcome—The horse responded well to do×ycycline treatment (10 mg/kg [4.5 mg/lb], PO, q 12 h for 60 days) and returned to normal exercise. However, 60 days after treatment was discontinued, the horse again developed a stiff neck and rapidly progressive neurologic deficits, including severe ataxia and vestibular deficits. The horse's condition deteriorated rapidly despite IV oxytetracycline treatment, and the horse was euthanatized. Postmortem examination revealed leptomeningitis, lymphohistiocytic leptomeningeal vasculitis, cranial neuritis, and peripheral radiculoneuritis with Wallerian degeneration; findings were consistent with a diagnosis of neuroborreliosis.

Clinical Relevance—Nervous system infection with B burgdorferi should be considered in horses with evidence of meningitis and high or equivocal serum anti-B burgdorferi antibody titers. Evaluation of immune function is recommended in adult horses evaluated because of primary bacterial meningitis.

Abstract

Case Description—A 12-year-old Thoroughbred was examined because of signs of depression, neck stiffness, and poor performance.

Clinical Findings—Physical examination revealed that the horse was dull, appeared depressed, was reluctant to raise its neck and head above a horizontal plane, and had a temperature of 38.5°C (101.3°F). No radiographic or scintigraphic abnormalities of the neck were found; however, high plasma fibrinogen concentration and relative lymphopenia were identified and the horse was seropositive for antibodies against Borrelia burgdorferi. Analysis of CSF revealed neutrophilic inflammation, and results of a PCR assay of CSF for B burgdorferi DNA were positive. Immunologic testing revealed severe B-cell lymphopenia and a low serum IgM concentration consistent with common variable immunodeficiency.

Treatment and Outcome—The horse responded well to do×ycycline treatment (10 mg/kg [4.5 mg/lb], PO, q 12 h for 60 days) and returned to normal exercise. However, 60 days after treatment was discontinued, the horse again developed a stiff neck and rapidly progressive neurologic deficits, including severe ataxia and vestibular deficits. The horse's condition deteriorated rapidly despite IV oxytetracycline treatment, and the horse was euthanatized. Postmortem examination revealed leptomeningitis, lymphohistiocytic leptomeningeal vasculitis, cranial neuritis, and peripheral radiculoneuritis with Wallerian degeneration; findings were consistent with a diagnosis of neuroborreliosis.

Clinical Relevance—Nervous system infection with B burgdorferi should be considered in horses with evidence of meningitis and high or equivocal serum anti-B burgdorferi antibody titers. Evaluation of immune function is recommended in adult horses evaluated because of primary bacterial meningitis.

Contributor Notes

Dr. James' present address is Donnington Grove Veterinary Surgery Oxford Rd, Newbury Berkshire, RG14 2JB, England.

The authors thank Dr. Julia Flaminio for assistance with immune function testing.

Address correspondence to Dr. James (franjames@donningtongrove.com).